Subsequent studies with the Mll-AF9 knock-in mouse line demonstrated pre- and postnatal stepwise progression of the disease [72], the role of the HOXA9 homeobox transcription factor as downstream effector [73] and gene dosage effects as well as putative cellular targets of MLL-AF9 to initiate AML [63]. This evidence concerns the gene MLLT3 and acute myeloid leukemia.